Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling
ABSTRACTPrevention of rotavirus (RV) infection by gut-resident segmented filamentous bacteria (SFB) is an example of the influence of gut microbiota composition on enteric viral infection. Yet, the mechanism by which SFB prevents RV infection is poorly understood. A recent report that SFB colonizati...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2023-12-01
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| Series: | Gut Microbes |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/19490976.2023.2174407 |
| _version_ | 1827303731039830016 |
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| author | Vu L. Ngo Zhenda Shi Baoming Jiang Andrew T. Gewirtz |
| author_facet | Vu L. Ngo Zhenda Shi Baoming Jiang Andrew T. Gewirtz |
| author_sort | Vu L. Ngo |
| collection | DOAJ |
| description | ABSTRACTPrevention of rotavirus (RV) infection by gut-resident segmented filamentous bacteria (SFB) is an example of the influence of gut microbiota composition on enteric viral infection. Yet, the mechanism by which SFB prevents RV infection is poorly understood. A recent report that SFB colonization of germfree mice generates retinoic acid (RA) thus activating RA receptor (RAR) signaling, which protected against Citrobacter rodentium infection, prompted us to investigate whether this pathway might contribute to SFB’s protection against RV infection. Colonization of conventional mice by SFB indeed increased intestinal RA levels and direct administration of RA partially mimicked the protection against RV infection conferred by SFB. Moreover, blockade of RAR signaling eliminated SFB’s protection against RV infection. Blockade of RAR signaling did not impact RV infection in the absence of SFB, nor did it alter the protection against RV infection conferred by bacterial flagellin, which in contrast to SFB, is dependent upon IL-22 signaling. SFB/RA-mediated prevention of RV infection was associated with an RA-dependent increase in enterocyte migration, consistent with the notion that enhanced anoikis is the ultimate means by which SFB, IL-22, and RA impede RV infection. |
| first_indexed | 2024-03-11T14:19:19Z |
| format | Article |
| id | doaj.art-74c33d56aab741fb83bb6524ae616245 |
| institution | Directory Open Access Journal |
| issn | 1949-0976 1949-0984 |
| language | English |
| last_indexed | 2024-04-24T17:07:19Z |
| publishDate | 2023-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Gut Microbes |
| spelling | doaj.art-74c33d56aab741fb83bb6524ae6162452024-03-28T22:38:20ZengTaylor & Francis GroupGut Microbes1949-09761949-09842023-12-0115110.1080/19490976.2023.2174407Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signalingVu L. Ngo0Zhenda Shi1Baoming Jiang2Andrew T. Gewirtz3Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USDivision of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USADivision of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USACenter for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USABSTRACTPrevention of rotavirus (RV) infection by gut-resident segmented filamentous bacteria (SFB) is an example of the influence of gut microbiota composition on enteric viral infection. Yet, the mechanism by which SFB prevents RV infection is poorly understood. A recent report that SFB colonization of germfree mice generates retinoic acid (RA) thus activating RA receptor (RAR) signaling, which protected against Citrobacter rodentium infection, prompted us to investigate whether this pathway might contribute to SFB’s protection against RV infection. Colonization of conventional mice by SFB indeed increased intestinal RA levels and direct administration of RA partially mimicked the protection against RV infection conferred by SFB. Moreover, blockade of RAR signaling eliminated SFB’s protection against RV infection. Blockade of RAR signaling did not impact RV infection in the absence of SFB, nor did it alter the protection against RV infection conferred by bacterial flagellin, which in contrast to SFB, is dependent upon IL-22 signaling. SFB/RA-mediated prevention of RV infection was associated with an RA-dependent increase in enterocyte migration, consistent with the notion that enhanced anoikis is the ultimate means by which SFB, IL-22, and RA impede RV infection.https://www.tandfonline.com/doi/10.1080/19490976.2023.2174407Retinoic acid receptornos2enterocyte migration |
| spellingShingle | Vu L. Ngo Zhenda Shi Baoming Jiang Andrew T. Gewirtz Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling Gut Microbes Retinoic acid receptor nos2 enterocyte migration |
| title | Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling |
| title_full | Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling |
| title_fullStr | Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling |
| title_full_unstemmed | Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling |
| title_short | Segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor-mediated signaling |
| title_sort | segmented filamentous bacteria impede rotavirus infection via retinoic acid receptor mediated signaling |
| topic | Retinoic acid receptor nos2 enterocyte migration |
| url | https://www.tandfonline.com/doi/10.1080/19490976.2023.2174407 |
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